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This Article Full Text Full Text (PDF) All Versions of this Article: 575/2/543    most recent jphysiol.2006.114108v2 jphysiol.2006.114108v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Cristofanilli, M. Articles by Akopian, A. Search for Related Content PubMed PubMed Citation Articles by Cristofanilli, M. Articles by Akopian, A. Related Collections Neuroscience

¹ Department of Ophthalmology, New York University School of Medicine, New York, NY 10016, USA

Intracellular Ca²⁺ regulates a variety of neuronal functions, including neurotransmitter release, protein phosphorylation, gene expression and synaptic plasticity. In a variety of cell types, including neurons, Ca²⁺ is involved in actin reorganization, resulting in either actin polymerization or depolymerization. Very little, however, is known about the relationship between Ca²⁺ and the actin cytoskeleton organization in retinal neurons. We studied the effect of high-K⁺-induced depolarization on F-actin organization in salamander retina and found that Ca²⁺ influx through voltage-gated L-type channels causes F-actin disruption, as assessed by 53 ± 5% (n = 23, P < 0.001) reduction in the intensity of staining with Alexa-Fluor488-phalloidin, a compound that permits visualization and quantification of polymerized actin. Calcium-induced F-actin depolymerization was attenuated in the presence of protein kinase C antagonists, chelerythrine or bis-indolylmaleimide hydrochloride (GF 109203X). In addition, phorbol 12-myristate 13-acetate (PMA), but not 4-PMA, mimicked the effect of Ca²⁺ influx on F-actin. Activation of ionotropic AMPA and NMDA glutamate receptors also caused a reduction in F-actin. No effect on F-actin was exerted by caffeine or thapsigargin, agents that stimulate Ca²⁺ release from internal stores. In whole-cell recording from a slice preparation, light-evoked ‘off’ but not ‘on’ EPSCs in ‘on–off’ ganglion cells were reduced by 60 ± 8% (n = 8, P < 0.01) by cytochalasin D. These data suggest that elevation of intracellular Ca²⁺ during excitatory synaptic activity initiates a cascade for activity-dependent actin remodelling, which in turn may serve as a feedback mechanism to attenuate excitotoxic Ca²⁺ accumulation induced by synaptic depolarization.

(Received 24 May 2006; accepted after revision 15 May 2006; first published online 15 May 2006)
Corresponding author A. Akopian: Department of Ophthalmology, New York University School of Medicine, 550 First Avenue PHL 843, New York, NY 10016, USA.  Email: aa3{at}nyu.edu

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